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DR: an endocrinologist’s view

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Professor Richard MacIsaac
BSc(Hons) PhD MBBS FRACP
Director, Department of Endocrinology & Diabetes, St Vincent’s Health, Melbourne & Professorial Fellow, University of Melbourne

 

Dr Geetha Theverkalam
MBBS DRANZCOG
Endocrinology Research Fellow, Department of Endocrinology & Diabetes, St Vincent’s Hospital & University of Melbourne

 

Diabetic retinopathy (DR) is the quintessential diabetes-related complication. The observed relationship between blood glucose levels and the presence of DR is used to identify the threshold glucose levels that define the presence of diabetes.1 DR, along with its associated complications, is the single most common and preventable cause of blindness in people with diabetes over 75 years of age. This emphasises the importance of the early detection of DR and the instigation of measures to prevent its development and progression.

Grading of DR


The National Health and Medical Research Council of Australia (NHMRC) guideline for the management of DR suggests using a five-stage grading system: no DR, minimal non-proliferative DR, mild to moderate DR, severe DR, and proliferative DR. Macular oedema is graded according to its absence or presence.2

Epidemiology


For patients with type 1 diabetes (T1DM), less than two per cent will have a DR lesion at diagnosis whereas 87-98 per cent will have an abnormality after 30 years of diabetes. For patients with type 2 diabetes (T2DM), 20-37 per cent will have a lesion at diagnosis but after 15 years of diabetes, 85 per cent on insulin and 60 per cent on oral agents will have a DR related abnormality. A global study involving 12,620 participants with diabetes has suggested that the prevalence of any form of DR is 35per cent with a prevalence of vision-threatening DR being 10 per cent.3

Risk factors for DR: ‘GLOBES’


The above study showed that diabetes duration, glycaemic control (glycated haemoglobin levels), blood pressure (BP) control and diabetes type (with the prevalence of diabetes being 77 per cent in T1DM versus 25 per cent in T2DM) were the major risk factors for DR. A simple acronym to help identify the risk factors for DR is ‘GLOBES’: glucoses, lipids, obesity, blood pressure, education status, smoking.

Screening for DR


Screening for DR and diabetes-related eye problems involves measurement of visual acuity, intraocular pressure, dilated fundoscopy, and/or retinal photography by an optometrist or an ophthalmologist. Screening for DR should be performed at the time of diagnosis with T2DM and within five years of the diagnosis of T1DM. The frequency of follow-up depends on the severity of DR. If no DR is detected or there are no significant risk factors, then the frequency of follow-up can be extended to three years. However, in high risk patients (using insulin, diabetes duration > 20 years or both), yearly screening is recommended. Even more frequent follow should occur in instances of rapid improvement in glycaemic control, puberty and pregnancy where acceleration of DR may occur.2

Management of DR: risk factor reduction


Randomised controlled trials have demonstrated that it is possible to improve diabetes-related eye outcomes with good glycaemic control. Primary prevention of DR with good glycaemic control is paramount in reducing risk of visual loss, whereas secondary prevention has a smaller effect but still remains effective. An emerging concept is that the beneficial effects of good glycaemic control continue to accrue over many years despite possible later deteriorations in glycaemic control. This concept is commonly referred to as ‘metabolic memory’.4,5

Other important contributing variables include aggressive management of BP and dyslipidaemia, and smoking cessation. Blocking the renin-angiotensin (R-A) system with an angiotensin converting enzyme (ACE) inhibitor or an angiotensin receptor blocker (ARB) has also been shown to slow the progression of DR. It is possible that this effect is due to a direct effect of blockade of the retinal R-A system independent of any BP lowering effects of ACE inhibitors or ARBs.6,7

Retinal photocoagulation


One of the main reasons for DR screening is the established effectiveness of retinal photo-coagulation in preventing visual loss. The Diabetic Retinopathy Study (DRS) demonstrated that pan-retinal photocoagulation was beneficial for reducing the risk of further visual loss in patients with proliferative DR.8 The Early Treatment Diabetic Retinopathy Study (ETDRS) also established the benefits of focal laser photocoagulation for patients with macular oedema.9

New treatment for DR


Fenofibrate, a medication that is usually used to lower triglyceride levels, has been approved by the Therapeutics Goods Authority (TGA) for the indication to slow the progression of existing DR in type 2 diabetes. This approval was based on the results of two large placebo, controlled trials that showed that the use of fenofibrate was associated with a reduction in the rate of progression of DR and the need for retinal photocoagulation.10,11 The effects of fenofibrate on the eye are independent of changes in lipid levels and likely involve an inhibition of growth factors or cytokines.12

The intra-vitreal injection of a recombinant monoclonal neutralising antibody to vascular endothelial growth factor (VEGF) improves vision and reduces the need for photocoagulation in patients with macular oedema. It is now a treatment that is being offered to patients in everyday clinical practice. Anti-VEGF treatment may also slow the progression of proliferative DR but this effect is yet to be established. Intra-vitreal delivery of fluocinolone is also another emerging therapy for the treatment of DR.1,2,13

Conclusion


Although the prevalence of diabetes continues to increase, which is mostly driven by an increase in type 2 diabetes, there is some good news regarding the eye health of patients with diabetes. In particular, better screening is yielding earlier detection and there are better treatments to control the risk factors for DR development and progression. Optometrists continue to play a vital role in the screening and management of diabetic eye disease.

 

  1. Standards of medical care in diabetes 2014. Diabetes Care 2014; 37 Suppl 1: S14-80.
  2. National Health and Medical Research Council, Guidelines for the Management of Diabetic Retinopathy. 2008.
  3. Yau JW, Rogers SL, Kawasaki R, Lamoureux EL, Kowalski JW, Bek T et al. Global prevalence and major risk factors of diabetic retinopathy. Diabetes Care 2012; 35: 3: 556-564.
  4. Holman RR, Paul SK, Bethel MA, Neil HA, Matthews DR. Long-term follow-up after tight control of blood pressure in type 2 diabetes. N Engl J Med 2008; 359: 15: 1565-1576.
  5. Aiello LP, Group DER. Diabetic retinopathy and other ocular findings in the diabetes control and complications trial/epidemiology of diabetes interventions and complications study. Diabetes Care 2014; 37: 1: 17-23.
  6. Chaturvedi N, Porta M, Klein R, Orchard T, Fuller J, Parving HH et al. Effect of candesartan on prevention (DIRECT-Prevent 1) and progression (DIRECT-Protect 1) of retinopathy in type 1 diabetes: randomised, placebo-controlled trials. Lancet 2008; 372: 9647: 1394-1402.
  7. Mauer M, Zinman B, Gardiner R, Suissa S, Sinaiko A, Strand T et al. Renal and retinal effects of enalapril and losartan in type 1 diabetes. N Engl J Med 2009; 361: 1: 40-51.
  8. Preliminary report on effects of photocoagulation therapy. The Diabetic Retinopathy Study Research Group. Amer J Ophthalmol 1976; 81: 4: 383-396.
  9. Photocoagulation for diabetic macular edema. Early Treatment Diabetic Retinopathy Study report number 1. Early Treatment Diabetic Retinopathy Study research group. Arch Ophthalmol 1985; 103: 12: 1796-1806.
  10. Keech AC, Mitchell P, Summanen PA, O’Day J, Davis TM, Moffitt MS et al. Effect of fenofibrate on the need for laser treatment for diabetic retinopathy (FIELD study): a randomised controlled trial. Lancet 2007; 370: 9600: 1687-1697.
  11. ACCORD Study Group et al. Effects of medical therapies on retinopathy progression in type 2 diabetes. New Eng J Medicine 2010; 363: 3: 233-244.
  12. Noonan JE, Jenkins AJ, Ma JX, Keech AC, Wang JJ, Lamoureux EL. An update on the molecular actions of fenofibrate and its clinical effects on diabetic retinopathy and other microvascular end points in patients with diabetes. Diabetes 2013; 62: 12: 3968-3975.
  13. Cheung N, Wong IY, Wong TY. Ocular anti-VEGF therapy for diabetic retinopathy: overview of clinical efficacy and evolving applications. Diabetes Care 2014; 37: 4: 900-905.


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